Biochemists Look to Proteins and Enzymes to Fight Cancer
Beradelli, Phil, Insight on the News
Of the many research paths that might lead to more effective cancer treatments, cell division may be the most promising. In humans as well as in all living organisms, normal cell development depends on a delicate biochemical balance. Disruption of that balance, often by invasive proteins or enzymes, can lead to unregulated or abnormal growth - cancer. The cell's ability to defend against these insidious substances is considered vital in the fight against the disease.
Researchers have uncovered potentially useful information about certain chemicals that repress or neutralize prime suspects in the development of tumors. Scientists at the Laboratory of Molecular Growth Regulation, part of the National Institutes of Health, or NIH, in Bethesda, Md., have isolated an enzyme they believe counteracts the effects of E1A, a virus-produced protein that seems to trigger cancer.
According to Yoshihiro Nakatani, a member of the NIH team, the enzyme, known as P/CAF, competes with E1A to attach to growth-control proteins. When E1A binds with the proteins, the host cell becomes a rogue, dividing much more rapidly than the surrounding tissue and developing its own textural characteristics. If the errant cells are not destroyed by the body's immune system, a tumor begins to form. But cloning P/CAF and increasing its strength within the cell can counteract E1A. That is, the enzyme can re-engage the cell's normal growth and tumor-suppression functions.
The discovery of P/CAF is considered significant in understanding oncoproteins, but it may be some time before it can be added to the arsenal of cancer-fighting weapons. Even though P/CAF can be synthesized, at present there is no practical way to deliver it to cells. "You simply can't drink it," says Nakatani, because it would be digested in the stomach. And injection would work only if the substance could be delivered to individual cells.
That leaves two alternatives: gene therapy and drugs. …